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210 oracic ultrasound
Finally, ultrasound plays a very interesting role in the mechanically ventilated patient, allowing
the bedside real time visualization of the effects of PEEP increases on the alveolar collapse
(Clips 38-42, 43-48).
Clips 38, 39, 40, 41, 42 – Alveolar collapse in a patient with ARDS
undergoing mechanical ventilation. Clip 38 documents the consolidation and
the presence of dynamic air bronchograms. The gradual increare of PEEP
(10 to 22 cm H
by the increase in air bronchograms. PEEP greater than 22 cm H
not change the situation. In this patient, the consolidation is therefore not
recruitable.
Clips 43, 44, 45, 46, 47, 48 – Alveolar collapse in a patient with
ARDS undergoing mechanical ventilation. PEEP is progressively increased
until full alveolar recruitment at 22 cm H
is recruitable.
O) only involves the recruitment of dead space, documented
2
O. In this patient, the consolidation
2
O did
2
ARDS and cardiogenic pulmonary edema
e differential diagnosis between ARDS and cardiogenic pulmonary edema is not easy and
has a different prognostic and therapeutic significance
129-131
.
At present, the differentiation of the two diseases is based on radiographic, echocardiographic
and CT findings, and finally, on the estimate of the capillary wedge pressure.
From the radiographic point of view, it is well-known that cardiogenic edema, unlike ARDS,
tends to show a inverted vascular distribution, a central or diffuse edema, Kerley B Lines,
pleural effusions and peribronchial cuffing.
Conversely, in ARDS edema tends to be peripheral or patchy. Moreover, ARDS shows peripheral consolidations with air bronchograms that are unusual in cardiogenic edema.
Echocardiography may suggest the cardiogenic nature of edema, when it highlights a severe
left ventricular systolic dysfunction or severe mitral aortic valve disease. However, it cannot
always provide immediate elements in the case of diastolic dysfunction
132
.
e echocardiographic estimation of pulmonary capillary wedge pressure, implemented with
various methods (transmitral flows, tissue Doppler, transmitral velocity of propagation), may
not be easy
133
.
A value of BNP less than 100 pg/ml virtually excludes the cardiac etiology of edema (“flash”
pulmonary edema may be an exception), but elevated BNP values (even > 500 pg/ml) are
possible in critically ill patients, in sepsis and in renal failure
134
.
Transthoracic ultrasonography plays a significant role in the differential diagnosis of the two
types of pulmonary edema. e algorithm in Figure 54 proposes an integrated approach for
the distinction between ARDS and cardiogenic pulmonary edema.
Parenchymal lung patology 211
PROBABLE
NON-CARDIOGENIC EDEMA
Sepsis, infections,
hyperleucocytosis
Pneumonia
Aspiration
Hyperdinamic state
Peritonitis, pancreatitis
BNP < 100 pg/mL
Normal heart volume
Peripheral infiltrates
Absence of Kerley B Lines
No flow variations
Air bronchograms
Inhomogeneous interstitial
syndrome with particularly
compact aspects
Presence of normal areas
Peripheral consolidations
Air bronchograms
Poor or no gliding
Lung pulse
No effusions
Normal or small cardiac
chambers
Normal left ventricular function
Patient with Acute
Pulmonary Edema
Clinical history, physical
examination, lab tests
CHEST X-RAY
CHEST
ULTRASOUND
PROBABLE CARDIOGENIC
EDEMA
Heart disease, IMA, failure
Peripheral edema
Low cardiac output
Pleural effusions
Increase in cardiac markers
BNP > 500-1000 pg/mL
Cardiomegaly
Pleural effusions
Central infiltrates
Poor or no peripheral
consolidations
Kerley B Lines
Absence of air bronchograms
Homogeneous interstitial
syndrome, first with thinned,
then compact B Lines
No peripheral consolidations
No bronchograms
Maintained gliding
Presence of effusions, even
small or minimal
Dilated heart
Compromised systolic or
dyastolic function
Wedge < o = 18 mm/Hg
Catheterization
pulmonary artery
Wedge > 18 mm/Hg
Figure 54 – Diagnostic algorithm useful for the differentiation between cardiogenic and noncardiogenic pulmonary edema.
Heart in ARDS
It has long been known that ARDS is frequently associated with pulmonary hypertension
and right ventricular dysfunction (RVD)
135-136
. ree conditions are mainly associated with
this situation. e first is due to lung injury, leading to a secondary alveolar dysfunction, to
destruction and thrombotic occlusion of capillaries. e second is related to vascular muscle hypertrophy, deriving from hypoxemia and hypercapnia. Finally, the positive pressure
212 oracic ultrasound
ventilation, which induces distal airways hypertension and compression of the capillaries.
ese phenomena are reversible, except for the destruction of the pulmonary capillaries.
A detrimental effect occurs more frequently when mechanical ventilation is performed with
high tidal volumes, aimed at the correction of PaCO2 and when the plateau pressure is not
limited.
Under these conditions, the RV dysfunction secondary to pulmonary hypertension, is common and is associated with higher mortality
137
.
Echocardiography plays a fundamental role, as it is able to detect dilation and RV systolic
dysfunction and the systolic paradox movement of the interventricular septum. Finally, the
degree of pulmonary hypertension can be assessed through the evaluation of the velocity of
tricuspid regurgitation
138
(Fig. 55) (Clip 49).
Figure 55 – Pulmonary hypertension in a patient with severe ARDS. Continuous-wave Doppler
sampling of tricuspid regurgitation shows a pressure gradient between the right ventricle and right atrium
of about 50 mmHg. The right atrial pressure calculated by evaluating the diameter of the inferior vena
cava and its in- and expiratory variations is around 14 mmHg. The systolic pressure in the pulmonary
artery is around 64 mmHg.
Clip 49 – Apical 4 chambers scan in a patient with ARDS, showing dilation
and severe right ventricular dysfunction.
e control of cardiopulmonary damage during mechanical ventilation is a big problem and
there are two possible ventilation strategies. One of them is defined “open-lung approach”,
and aims to achieve high in- and expiratory pressures in order to better recruit the lung.
However, it likely undermines the right ventricle. e other one is defined “RV protective
approach”, more aimed at the protection of the right ventricle.
Many studies have shown that the appearance of right ventricular dysfunction represents a
major negative prognostic factor of ARDS
139
.
Parenchymal lung patology 213
ese data suggest the need for an echocardiographic monitoring (daily, especially in severe
forms) of RV function, with immediate interventions on the ventilation mode (reduction of the
plateau pressure, PEEP and prone ventilation), if signs of acute cor pulmonale should appear
140
.
➣ Venous thromboembolic disease (VTD)
is term is inclusive of deep vein thrombosis and pulmonary embolism. VTD is a disease
with high morbidity and mortality. It is estimated that the average annual incidence of VTD is
70-113 per 100,000 person. In the U.S., it counts 250,000 annual incident cases. Approximately
one third of patients with symptomatic VTD manifest pulmonary embolism (PE), whereas
two third manifest deep vein thrombosis (DVT) alone. Death occurs in 6% of DVT cases and
12% of PE cases within one month of diagnosis. Studies that include a large number of VTD
cases diagnosed by autopsy generally report a higher proportion of cases with PE than DVT.
erefore, it is probable that reliance on clinical diagnosis underestimates the real incidence of
PE. is disease is a major health problem in Europe, with 370,000 annual deaths related to
pulmonary embolism.
e incidence of deep vein thrombosis is approximately three times that of pulmonary embolism,
and is its largest causal factor. Pulmonary embolism can be symptomatic and rapidly fatal or it
can cause chronic pulmonary hypertension of thromboembolic genesis
In this section we discuss the basis of general and ultrasound diagnosis of pulmonary embolism,
pointing out the evaluation of dyspnoic, or hemodynamically unstable patient. e next will
discuss deep vein thrombosis.
e diagnosis of pulmonary embolism without shock is not simple. During chest ultrasound
examination, pulmonary embolism may not show any sign. e diagnostic procedure, in these
cases, essentially uses the pretest probability of disease associated with compatible symptoms,
echocardiographic signs, in the absence of pleuropulmonary signs of another causal disease. When
there is no lung or pleural ultrasound sign, the ultrasonography with venous compression of
the lower limbs (CUS) plays an important role in detecting a DVT.
However, it is possible that the symptoms and clinical signs of pulmonary embolism occur with
positive sonographic findings, suggestive of this disease. In our opinion, these events are late, often
recurrent, such as to produce small multiple pulmonary consolidations.
141-144
.
Pulmonary embolism (PE)
Symptoms of PE occur even in the absence of physical, radiographic or echocardiographic
findings. erefore, often PE is not diagnosed early or is entirely unrecognized
145-148
. Autopsy
studies indicate that approximately 73% of pulmonary emboli diagnosed postmortem has
never had a clinical diagnosis during the course of the disease. For this reason, PE is an insidious disease, sometimes difficult to diagnose with a very important impact especially in certain
categories of patients.
Venous thromboembolic disease shows a prevalence in males with a high mortality rate (15
to 17.5% after three months from the event). It is estimated that in the U.S. pulmonary
embolism constitutes the third leading cause of death and causes 250,000 hospitalizations
annually with about 50,000 deaths.
More than 90% of emboli that reach the lungs arise from thrombi located in the deep veins
of the lower limbs (DVT) and approximately 40% of patients with DVT, even in the absence
of embolic symptoms, shows perfusion defects on lung scan. In contrast, among patients with
214 oracic ultrasound
pulmonary embolism, only 29% has ultrasound abnormalities of the deep venous trunks of
the lower limbs.
e diagnostic uncertainties of thromboembolic disease also lie in the fact that more than 50%
of patients with signs and symptoms in the lower limbs (pain, edema), suggestive of DVT,
recognizes different diseases, and is therefore exposed to the risk of unnecessary treatment.
Table 16 lists the risk factors for the thromboembolic disease
149
. eir detection during the
medical history and physical examination is important and allows to identify patients at low,
intermediate or elevate risk
interpretation of subsequent blood and instrumental tests
150
. is stratification has practical implications especially in the
.
e symptoms of pulmonary embolism are not constant nor specific. Pulmonary embolism
should be suspected in all patients with dyspnea, chest pain or hypotension, without apparent
cause. Dyspnea, pleuritic pain and cough are the symptoms encountered most frequently, while
hemoptysis occurs only occasionally. e clinical signs include tachycardia and tachypnea.
Patients with massive PE may instead manifest syncope, cardiovascular collapse or shock
146
In pulmonary embolism, chest X-ray is not particularly useful, and in 40% of cases it is
normal. Its main usefulness lies in suggesting alternative diagnoses such as pneumonia, tumors or heart failure. Occasionally, this examination may show an obvious focal oligoemia
(Westermark sign), peripheral consolidations or a right ectasic descending pulmonary artery.
Inverted waves in the precordial leads (V1-V4) are the most frequent ECG abnormality, while
the development of a right bundle branch block or of an atrial fibrillation is not common.
ECG S1-Q3 aspect and inverted T wave in lead III is not a constant finding.
Rarely the analysis of arterial blood gas has a diagnostic value. Recent studies indicate that, in
the absence of other cardiopulmonary diseases, more than 30% of patients with pulmonary
embolism have oxymetric values greater than 80 mmHg. Moreover, the degree of mismatch
between ventilation and perfusion is too variable to generate significant and constant gas
anomalies, especially in minor embolic forms.
Since physical examination, blood gas data, radiographic findings and ECG have low diagnostic accuracy, the strategy to diagnose PE must be sequential. Usual learning dictates
that the probability of disease is the primary diagnostic point. e dosage of high sensitivity
D-dimer is highly accurate only in specific cases. Finally, the gold standard for diagnosing
PE is the CT pulmonary angiography.
D-dimer assay (ELISA test) is highly sensitive (97-99%) for thromboembolic disease, and it
allows with reasonable accuracy the exclusion of an embolic event in hemodynamically stable
cases with low or moderate pretest probability, but it has low specificity. In these categories
of patients, its negativity avoids further investigation. Hemodynamically stable patients with
low or moderate pretest probability of PE, in the absence of anticoagulation, have a risk of
thromboembolism of 0.14%.
Hemodynamically stable patients with high risk of pulmonary embolism or with elevated
D-dimer values must undergo CT angiography. e negative predictive power of this evaluation is approximately 95%. CT negativity in these subjects, in the absence of anticoagulation,
produces a risk of thromboembolism at three months of approximately 1.5%, which drops
to 0.5% with the normal values of D-dimer.
e ventilation/perfusion scintigraphy may be useful for the diagnosis of pulmonary embolism
in the absence of CT angiography or if it is impossible to administrate the contrast agent.
It makes evident the regions where there is a decoupling between ventilation and perfusion.
.
Parenchymal lung patology 215
Table 16 – Risk factors for the thromboembolic disease
Venous stasis
Immobility
Recent surgery
Pregnancy or childbirth
Pelvic masses
Thrombophilia
Congenital causes
Prothrombin gene mutation
Antithrombin III deficiency
Deficiency of protein C and protein S deficiency
Leyden Factor V
High levels of factor VIII
Hyperhomocysteinemia
Dysfibrinogenemia
Acquired causes
Chronic medical illnesses
Heparin-induced thrombocytopenia
Inflammatory bowel disease
Tumors
Antiphospholipid syndrome
myeloproliferative disorders
Oral contraceptives
Nephrotic syndrome
Hormone replacement therapy
Paroxysmal nocturnal hemoglobinuria
Miscellaneous
Age
Hyperviscosity syndrome
History of thromboembolic disease
Generic familiarity for thromboembolic disease
Hypertension
Cigarette smoking
Central venous catheters, pacemaker electrodes
Air travel
Body mass index > 30
216 oracic ultrasound
e normal scintigraphy excludes pulmonary embolism (negative predictive value 97%). A
scintigraphy with highly probable signs of embolism has a positive predictive value of 85 to
90%. Pretest clinical suspicion and the existence of a venous thrombosis increases the possibility that subjects with abnormal images actually have pulmonary embolism
151-153
.
Tables 17 and 18 show the probability score for venous thrombosis and pulmonary embolism.
Table 17 – Probability score for venous thrombosis
Clinical aspects Score
Active neoplasm
Paralysis, paresis or recent plaster cast immobilization of the lower extremities
Recent bed immobilization (> 3 days) or major surgery within 12 previous weeks
Elective pain along the major venous trunks
Swelling of the entire limb
Calf swelling > 3 cm compared to the contralateral
Pitting edema
Superficial venous collateral circulation (not varicose)
Plausible alternative diagnosis
High pretest probability: ≥ 2 points
Low pretest probability: < 2 points
Modified from Wells PS
N Engl J Med
2003; 349: 1227-1235.
et al.
Evaluation of D-dimer in the diagnosis of suspected deep-vein thrombosis.
1
1
1
1
1
1
1
1
-2
Table 18 – Probability score for pulmonary embolism
Clinical aspects Score
Signs and symptoms of venous thrombosis
Heart rate > 100/min
Immobilization (> 3 consecutive days)
Surgery in the previous 4 weeks
Previous diagnosis of venous thrombosis or pulmonary embolism
Hemoptysis
Neoplasm
Pulmonary embolism with probability equal to or greater than another
diagnosis
High probability: > 6 points
Intermediate probability: 2-6 points
Low probability: < 2 points
Modified from Wells PS
management of patients with suspected pulmonary embolism presenting to the emergency department
by using a simple clinical model and D-dimer.
et al.
Excluding pulmonary embolism at the bedside without diagnostic imaging:
Ann Intern Med
2001; 135: 98-107.
3
1.5
1.5
1.5
1.5
1
1
3
e diagnostic accuracy of radionuclide scan does not arise when scintigrams and the pretest probability of disease are high or low. It arises when scintigraphy gives results with an
intermediate probability of embolization in the face of uncertain clinical data. It is likely that
these cases represent up to 50% of the total number of subjects and therefore scintigraphy, in
a significant number of cases, has to be complemented by further diagnostic investigations.
Parenchymal lung patology 217
Table 19 represents the data obtained from the PIOPED study and related to the correlation
between ventilation-perfusion lung scintigraphy and the pretest probability derived from
clinical data.
Table 19 – Correlation between the results of ventilation-perfusion lung scintigraphy and the clinical
pretest probability
Data relating to
scintigraphy
High probability
Intermediate probability
Low probability
Normality
Total
Clinical probability of embolism (%)
High (80-100%) Intermediate (20-79%) Low (0-19%) Total
96
66
40
00
68 30 09 28
88
28
16
06
56
16
04
02
87
30
14
04
Prognostic factors
154-156
Patients with pulmonary embolism should be classified according to the risk of adverse events
during the early stages of the disease. Hemodynamic instability is a major negative prognostic
factor for survival. e mortality rate rises from 15% of patients stable to around 58% of
those with hemodynamic instability. e echocardiographic right ventricular dysfunction,
and especially hypokinesia and dilatation of the right ventricle are independent predictors
of mortality in hemodynamically stable subjects. It has been shown that high values of BNP
and pro-BNP affect the intra-hospital outcomes of patients. Normal values of these markers have a negative predictive value close to 100% with for adverse events in subjects with
haemodynamically stable pulmonary embolism. Elevated levels of troponin also have a similar
negative meaning.
e ultrasound approach to pulmonary embolism is algoryhtmic and multidistrict. A normal
lung pattern in a symptomatic patient with probability for embolism should lead to the search
for positive sonographic signs of pulmonary embolism. However, regardless of the negativity
of these findings, it should lead to a multidirectional diagnostic strategy (see below) with the
search for signs of right ventricular dysfunction. e absence of right ventricular dysfunction and low level of troponin, BNP or pro-BNP identifies low risk patients. Signs of right
ventricular dysfunction identify subjects with submassive or massive pulmonary embolism
(differentiated on the basis of hemodynamic stability). Finally, findings of lung without interstitial disease and absence of pleural or consolidating disease, but with high values of BNP or
pro-BNP, are very important. is dissociation could indicate right ventricular strain without
pulmonary congestion, and a possible pulmonary embolism (high risk).
Figure 56 shows the clinical management in case of confirmed pulmonary embolism. It is
interesting to note that the risk stratification decisively influences the course of treatment
157
.
Positive sonographic findings for pulmonary embolism
e role of lung ultrasound in pulmonary embolism, although identified since the late six-
158-159
ties
, had little relevance in the literature. Since the arterial vascularization of the lung
cannot be visualized by ultrasound, we can detect in alveolar consolidation the basis for the
visualization of a PE. erefore, ultrasound can identify only secondary signs of PE. If this
occurs, ultrasound shows the consequences of the embolus in the parenchyma and not the
vascular obstruction. ese issues have been well described by Mathis and coll.
80,160-163
.
218 oracic ultrasound
CLINICAL FINDINGS
Shock or prolonged hypotension
Systolic blood pressure <90mmHg
Reduction in blood pressure ≥40mmHg for over 15’
Unstable hemodynamics Stable hemodynamics
Thrombolysis, surgery,
transcatheter thromboaspiration
No right ventricular dysfunction
No myocardial injury
Anticoagulation
Consider brief hospitalization
Consider treatment at home
Right ventricular dysfunction
Anticoagulation
Hospitalization in medical
environment
Clinical and echocardiographic
assessement
Assessment of right ventricular
dysfunction
Echocardiogram
Angio-CT
Dosage Troponins for myocardial
injury of the right ventricle
Right ventricular dysfunction
Myocardial injury
Hospitalization in ICU
Consider thrombolysis in patients
at low risk of bleeding
Figure 56 – Management of confirmed pulmonary embolism (modified from: Agnelli G, Becattini C.
Acute pulmonary embolism.
N Engl J Med
2010; 363: 266-274).
e physiopathology of pulmonary vascular occlusion is well known. e embolic occlusion
causes the loss of alveolar surfactant in the area depending from the occluded vessel. e
infiltration of interstitial fluid and of erythrocytes in the lumen of the alveoli and alveolar
collapse is its consequence. e absence of air in the alveoli then allows the ultrasound beam
to explore the lesion.
e frequency of consolidative lesions (infarcts) of the lung parenchyma in the case of embolism varies between 25% and 60%. However, pulmonary embolism is a highly dynamic
process and it is known that subpleural consolidations have a high frequency in CT. ey do
not always appear as necrosis, but rather as atelectasis or small exudative consolidations
164
.
In ultrasound, they take on different aspects. If recent, they are hypoechoic and homogeneous wedge-shaped consolidations. Characteristically, these lesions are adjacent to the pleura
with their more expanded portion. Often show a convex pleural contour, that almost raises
the serosa which is often interrupted or at least fragmented.
eir average size is 13 x 10 mm (range 5-70 mm), and the shape is rounded (11%) or polygonal (4%), with blurred or defined boundaries with respect to the adjacent parenchyma.
Parenchymal lung patology 219
Lesions smaller than 5 mm can hardly be distinguished from pleural scarring or fibrotic
nodules
165-170
.
Embolic consolidations contain little air for the hypoxic constriction of the afferent bronchus
and/or for the compression by the exudate. In recent embolism it is rare to see a clear air
bronchogram.
Instead, older infarcts are better demarcated, wedge-shaped and with central echoes corresponding to the bronchiole, indicating their segmental nature.
Very rarely the congested embolized vessel can be seen (vessel sign) as a tubular transonic
structure.
In two thirds of cases, the localization of the embolic lesions is at the level of the dorsal segments of the lower lobes. eir multiplicity associated with a high clinical probability for
embolism, makes ultrasound accurate in over 90% of cases.
Finally, a layer of radio-occult pleural effusion is detected (50-60%) in the basal regions. Other
times, an enlarged pleural space containing fluid (“sentinel effusion”) is seen at the level of
the lesion (Figs. 57-60) (Clips 50-51).
SENTINEL FLUID
PULMONARY INFARCTION
Figure 57 – Small triangular pulmonary infarction. A “sentinel” effusion in the contiguous pleural
space is evident.
Figure 58 – Lung in massive of pulmonary embolism, at least in the early stages, can appear perfectly
normal on ultrasound (right).
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